6a. Fever in adults Flashcards
1
Q
history
A
2
Q
exam
A
3
Q
ddx
A
4
Q
buffer
A
5
Q
buffer
A
6
Q
buffer
A
7
Q
what is sepsis?
A
life-threatening organ dysfunction caused by a dysregulated host response to an infection
8
Q
what is septic shock, how should it be treated?
A
a more severe form sepsis, technically defined as ‘in which circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone
Septic shock is defined when arterial blood pressure drops and results in organ hypo-perfusion. This leads to a rise in blood lactate as the organs begin anaerobic respiration. This can be measured as either:
Systolic blood pressure less than 90 despite fluid resuscitation
Hyperlactaemia (lactate > 4 mmol/L)
This should be treated aggressively with IV fluids to improve the blood pressure and the tissue perfusion. If IV fluid boluses don’t improve the blood pressure and lactate level then they should be escalated to high dependency or intensive care where they can use medication called inotropes (such as noradrenalin) that help stimulate the cardiovascular system and improve blood pressure and tissue perfusion.
9
Q
what score can be used outside ICU to assess a patients risk of mortality from sepsis if there is a ?infection
A
qSOFA
Respiratory rate > 22/min
Altered mentation
Systolic blood pressure < 100 mm Hg
qSOFA Scores 2-3 are associated with a 3- to 14-fold increase in in-hospital mortality. Assess for evidence of organ dysfunction with blood testing including serum lactate and calculation of the full SOFA Score.
Patients meeting these qSOFA criteria should have infection considered even if it was previously not.
10
Q
red flags for sepsis ?
A
2,3,4
Behaviour:
- responds only to voice or pain/unresponsive
- acute confusional state
Vital signs:
- systolic bp <90 or drop of >40 from normal
- heart rate >130
- RR >25
Additional signs:
- non blanching rash, mottled, ashen, cyanotic
- not passed urine in last 18hr/ UO < 0.5ml/kg/hr
- lactate > 2
- recent chemo
11
Q
when should the sepsis 6 be started?
A
when there are any red flags/ there is a suspicion of sepsis
12
Q
what are the sepsis 6?
A
- Administer oxygen: Aim to keep saturations > 94% (88-92% if at risk of CO2 retention e.g. COPD)
- Take blood cultures
- Give broad-spectrum antibiotics
- Give intravenous fluid challenges
NICE recommend a bolus of 500ml crystalloid over less than 15 minutes - Measure serum lactate
- Measure accurate hourly urine output
13
Q
what is the SOFA score
A
used in ICU for patients ?sepsis
A SOFA score of 2 or more reflects an overall mortality risk of approximately 10% in a general hospital population with suspected infection.
14
Q
amber flags for sepsis
A
- relatives concerned about mental status
- acute deterioration in functional ability
- immunosuppressed
- trauma/surgery/procedure in last 6 weeks
- rr 21–24
- systolic bp 91-100
- heart taye 91-130 or new dysrhythmia
- not passed urine in last 12-18 hours
- temp <36
- clinical signs of wound, device or skin infection
15
Q
risk factors for sepsis
A
extremes of age; people who are frail, immunocompromised or immunosuppressed; people who have had recent trauma or surgery; people with a breach in skin integrity; and women who are pregnant, are post-partum, or have had a recent termination of pregnancy or miscarriage.
16
Q
what are the sepsis 7 and 8
A
- Transfer to critical care may be needed to assess the need for central venous access and initiation of inotropes (increase cardiac output by increasing cardiac contractility) or vasopressors (increase blood pressure by increasing peripheral vascular resistance), to maintain perfusion pressure.
- Finding a source:
FBC: WCC may be high or low, thrombocytopaenia may indicate DIC
CRP - infection or inflamamtion
Creatinine, urea and electrolytes - dehydration, aki
LFTs - increased bilirubin or alanine aminotransferase (ALT) levels may indicate cholestasis or other liver dysfunction.
Clotting screen — if abnormal may indicate coagulopathy/DIC.
Urine analysis and culture, chest X-ray, CT for intra-abdo infection or abscess, LP for meningitis/encephalitis
additional investigations depending on the person’s clinical presentation — this may allow identification of the source of infection, pathogen(s) and sensitivities, and subsequent tailoring and/or de-escalation of antibiotic therapy if appropriate. Source control to eliminate a focus of infection may be possible, such as abscess drainage, debridement of infected tissue, removal of infected devices or foreign bodies, or surgery.
17
Q
what is neutropenic sepsis
A
It is sepsis in a patient with a low neutrophil count of less than 1 x 109/L.
Low neutrophil counts are usually the consequence of anti-cancer or immunosuppressant treatment.
18
Q
drugs that can cause neutropenia
A
Anti-cancer chemotherapy
Clozapine (schizophrenia)
Hydroxychloroquine (rheumatoid arthritis)
Methotrexate (rheumatoid arthritis)
Sulfasalazine (rheumatoid arthritis)
Carbimazole (hyperthyroidism)
Quinine (malaria)
Infliximab (monoclonal antibody use for immunosuppression)
Rituximab (monoclonal antibody use for immunosuppression)
19
Q
recognition and management of neutropenic sepsis ?
A
Have a low threshold for suspecting netropenic sepsis in patients taking immunosuppressants or medications that can cause neutropenia
Treat any temperature above 38C as neutropenic sepsis in these patients until proven otherwise.
Treatment is with immediate broad spectrum antibiotics such as piperacillin with tazobactam (tazocin).
The other aspects of management are essentially the same as for sepsis however extra precaution needs to be taken. Time is precious so don’t delay antibiotics while waiting for investigation results.
20
Q
pyrexia of unknown origin
A
21
Q
buffer
A
22
Q
buffer
A
23
Q
buffer
A
24
Q
buffer
A
25
buffer
26
what are some skin and soft tissue infections?
- cellulitis
- necrotising fasciitis
- scabies is a skin infection
27
what is cellulitis
Cellulitis is a bacterial infection that affects the dermis and the deeper subcutaneous tissues.
28
features cellulitis
Erythema (red discolouration)
Warm or hot to touch
Tense
Thickened
Oedematous
Bullae (fluid-filled blisters)
A golden-yellow crust can be present and indicate a staphylococcus aureus infection
commonly occurs on the shins
usually unilateral - bilateral cellulitis is rare and suggests an alternative diagnosis
systemic upset
fever
malaise
nausea
29
most common causative agent cellulitis
Streptococcus pyogenes
or less commonly Staphylococcus aureus
30
what classification is used to guide management of patients with cellulitis
Eron classification
31
Eron classification of cellulitis
I There are no signs of systemic toxicity and the person has no uncontrolled co-morbidities
II The person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection
III The person has significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize
IV The person has sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis
32
who should be admitted with cellulitis
Has Eron Class III or Class IV cellulitis.
Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
Is very young (under 1 year of age) or frail.
Is immunocompromised.
Has significant lymphoedema.
Has facial cellulitis (unless very mild) or periorbital cellulitis.
33
how to manage eron class 2 cellulitis
Admission may not be necessary if the facilities and expertise are available in the community to give intravenous antibiotics and monitor the person - check local guidelines.
34
how to manage eron class 1 cellulitis? 1st line? other options?
oral antibiotics
1. oral flucloxacillin as first-line treatment for mild/moderate cellulitis
oral clarithromycin, erythromycin (in pregnancy) or doxycycline is recommended in patients allergic to penicillin
35
how to manage class 3 and 4 cellulitis
admit usually for IV abx
oral/IV co-amoxiclav, oral/IV clindamycin, IV cefuroxime or IV ceftriaxone
36
Pre-septal/perioribital vs orbital cellulitis
Preseptal cellulitis is sometimes also referred to as periorbital cellulitis. It is an infection of the soft tissues anterior to the orbital septum - this includes the eyelids, skin and subcutaneous tissue of the face, but not the contents of the orbit.
This is in contrast to orbital cellulitis, which is an infection of the soft tissues behind the orbital septum, and is a much more serious infection.
Orbital signs (pain on movement of the eye, restriction of eye movements, proptosis, visual disturbance, chemosis, RAPD) must be absent in preseptal cellulitis - their presence would indicate orbital cellulitis
37
epidemiology preseptal celulitis and orbital cellulitis
- Preseptal cellulitis occurs most commonly in children - 80% of patients are under 10 and the median age of presentation is 21 months
- It is more common in the winter due to the increased prevalence of respiratory tract infections.
orbital cellulitis - Mean age of hospitalisation 7-12 years
38
Management of preseptal and of orbital cellulitis
1. Refer to secondary care, orbital is much more time critical
1. CT with contrast to differentiate between
+ FBC, blood culture, swab of any discharge
Periorbital: often oral co-amoxiclav and observation
Orbital: IV abx
39
what often precedes periorbital/orbital cellulitis
sinus infection, facial infection, insect bite
40
most common causative organisms preseptal/orbital cellulitis
Staph. aureus, Staph. epidermidis, streptococci and anaerobic bacteria
41
types of necrotising fasciitis
It can be classified according to the causative organism:
type 1 is caused by mixed anaerobes and aerobes (often occurs post-surgery in diabetics). This is the most common type
type 2 is caused by Streptococcus pyogenes
42
features of necrotising fasciitis
acute onset
pain, swelling, erythema at the affected site
often presents as rapidly worsening cellulitis with pain out of keeping with physical features
extremely tender over infected tissue with hyperaesthesia to light touch
skin necrosis and crepitus/gas gangrene are late signs
fever and tachycardia may be absent or occur late in the presentation
43
risk fasctors necrotising fasciitis
skin factors: recent trauma, burns or soft tissue infections
diabetes mellitus is the most common preexisting medical condition, particularly if the patient is treated with SGLT-2 inhibitors
intravenous drug use
immunosuppression
44
most common affected site necrotising fasciitis
the perineum (Fournier's gangrene)
45
management necrotising fasciitis
urgent surgical referral debridement
intravenous antibiotics
46
prognosis necrotising fasciitis
average mortality of 20%
47
severe itch with skin marks and scratch marks present for 2 weeks and getting worse, itch worse at night time- impacting sleep,
scabies
48
typical history and examination scabies
PC: severe itch with skin marks and scratch marks present for 2 weeks and getting worse
HoPC: itch worse at night time- impacting sleep,
Red flags: no fever, no weight loss, some fatigue but thinks this is due to reduced sleep due to itch, no night sweats, no lumps
MHx: none
DHx: none
Allergies: nkda
FHx: none
SHx: 1st year at uni, new sexual partner also experiencing severe itch
ICE: sleep is severely affected and is affecting uni work, skin marks affecting confidence, concerned it is infectious as her partner is having the same problem - is embarrassed to talk to anyone about it
o/e: Widespread erythematous papules on fingers, front of torso, genitalia, extensor surfaces of arms, scratch marks, thread-like tracks measuring around 5–10 mm in between fingers,
49
pathophysiology scabies
Scabies is a transmissible skin disease caused by the ectoparasitic mite Sarcoptes scabiei var. Hominis.
Itch is due to a delayed type-IV hypersensitivity reaction to the mite and mite products (faeces and eggs) so symptoms appear 4-6 weeks after infection.
50
Typical history common cold
PC: runny nose, sneezing, watery eyes, postnasal drip, fatigue, low grade fever, dry cough
HoPC: no SOB, no wheeze
51
what is the common cold?
The common cold is an acute, self-limiting, viral inflammation of the mucosa of the upper respiratory tract. The common cold actually describes an array of similar conditions caused by a vast number of different viruses. It is most often caused by infection with rhinoviruses (50-80%) and coronaviruses
52
most common pathogen common cold
rhinoviruses
53
management common cold?
Symptomatic:
Steam inhalation
Gargle salt water
paracetamol/ibuprofen
safety net
54
What is bronchitis?
Acute bronchitis is a type of chest infection which is usually self-limiting in nature.
It is a result of inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum.
55
typical history and EXAM bronchitis?
PC: cough: may or may not be productive, sore throat, rhinorrhoea, wheeze
o/e: no other focal chest signs other than wheeze
56
Management bronchitis
analgesia
good fluid intake
consider antibiotic therapy if patients:
- are systemically very unwell
- have pre-existing co-morbidities
- have a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
NICE Clinical Knowledge Summaries/BNF currently recommend doxycycline first-line
doxycycline cannot be used in children or pregnant women
alternatives include amoxicillin
57
Presentation of flu?
Rapid onset of:
Fever
Coryzal symptoms
Lethargy and fatigue
Anorexia (loss of appetite)
Muscle and joint aches
Headache (retro-orbital)
Dry cough
Sore throat
58
what is flu?
illness caused by the influenza virus =
an RNA virus
59
management of flu?
1. check if PH reccomend treatment
Public health monitor the number of cases of flu and provide guidance on when there is enough flu in the area to justify treating patients with suspected flu.
2. Healthy patients that are not at risk of complications do not need treatment with antiviral medications. The infection will resolve with self care measures such as adequate fluid intake and rest.
3. There are two options for treatment in someone presenting with suspected influenza that is at risk of complications of influenza:
Oral oseltamivir 75mg twice daily for 5 days
Inhaled zanamivir 10mg twice daily for 5 days
Treatment needs to be started within 48 hours of the onset of symptoms to be effective.
60
post-exposure prophylaxis flu
Post-exposure prophylaxis can be given to higher risk patients such as those with chronic diseases or immunosuppression within 48 hours of close contact with influenza. This aims to minimise the risk of developing flu and complications.
Oral oseltamivir 75mg once daily for 10 days
Inhaled zanamivir 10mg once daily for 10 days
61
complications of flu?
Otitis media, sinusitis and bronchitis
Viral pneumonia
Secondary bacteria pneumonia
Worsening of chronic health conditions such as COPD and heart failure
Febrile convulsions (young children)
Encephalitis
62
children influenza vaccination program?
- it is given intranasally
- the first dose is given at 2-3 years, then annually after that
- it is a live vaccine
dont give if ill or allergic to eggs
if immunosuppressed give injectable (not live) vaccine
63
adults influenza vaccination program?
annual influenza vaccination for all people older than 65 years, and those older than 6 months if they have:
chronic respiratory disease (including asthmatics who use inhaled steroids)
chronic heart disease (heart failure, ischaemic heart disease, including hypertension if associated with cardiac complications)
chronic kidney disease
chronic liver disease: cirrhosis, biliary atresia, chronic hepatitis
chronic neurological disease: (e.g. Stroke/TIAs)
diabetes mellitus (including diet controlled)
immunosuppression due to disease or treatment (e.g. HIV)
asplenia or splenic dysfunction
pregnant women
adults with a body mass index >= 40 kg/m²
health and social care staff directly involved in patient care (e.g. NHS staff)
those living in long-stay residential care homes
carers of the elderly or disabled person whose welfare may be at risk if the carer becomes ill (at the GP's discretion)
64
when is influenza season? when should vaccine be given?
starts in november
vaccinate ideally between sep and early nov
65
what is pneumonia
Infection of lung tissue → inflammation → sputum filling airways
66
what is community aquired pneumonia (CAP)?
develops outside hospital or within 48 hours of hospital admission
67
what is hospital aquired pneumonia (HAP)?
develops more than 48 hours after hospital admission
or within 30 days of a hospital admission
68
what is aspiration pneumonia
develops as a result of aspiration - inhaling foreign material such as food
69
typical history and examination pneumonia?
PC: SOB, cough productive of sputum, fever, haemoptysis, pleuritic chest pain, delirium, sepsis
o/e: tachypnoea, tachycardia, hypoxia, hypotension, fever, confusion
Bronchial breath sounds - harsh breath sounds equally loud on inspiration and expiration
Focal coarse crackles - air passing through sputum
Dullness to percussion - due to lung collapse and/or consolidation
70
what scoring system is used in priamry care for pneumonia ? how do you interpret?
CRB65 criteria:
Criterion Marker
C Confusion (abbreviated mental test score <= 8/10)
R Respiration rate >= 30/min
B Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg
65 Aged >= 65 years
Patients are stratified for risk of death as follows:
0: low risk (less than 1% mortality risk) NICE recommend that treatment at home should be considered (alongside clinical judgement)
1 or 2: intermediate risk (1-10% mortality risk) NICE recommend that ' hospital assessment should be considered (particularly for people with a score of 2)'
3 or 4: high risk (more than 10% mortality risk) NICE recommend urgent admission to hospital
71
interpretation of point of care CRP test for penumonia
NICE also mentioned a point-of-care CRP test. This is currently not widely available but they make the following recommendation with reference to the use of antibiotic therapy:
CRP < 20 mg/L - do not routinely offer antibiotic therapy
CRP 20 - 100 mg/L - consider a delayed antibiotic prescription
CRP > 100 mg/L - offer antibiotic therapy
72
what scoring system is used for pneumonia in secondary care? interpretation?
Criterion Marker
C Confusion (abbreviated mental test score <= 8/10)
U urea > 7 mmol/L
R Respiration rate >= 30/min
B Blood pressure: systolic <= 90 mmHg and/or diastolic <= 60 mmHg
65 Aged >= 65 years
NICE recommend, in conjunction with clinical judgement:
consider home-based care for patients with a CURB65 score of 0 or 1 - low risk (less than 3% mortality risk)
consider hospital-based care for patients with a CURB65 score of 2 or more - intermediate risk (3-15% mortality risk)
consider intensive care assessment for patients with a CURB65 score of 3 or more - high risk (more than 15% mortality risk)
73
Investigations ?pneumonia
chest x-ray
in intermediate or high-risk patients NICE recommend blood and sputum cultures, pneumococcal and legionella urinary antigen tests
CRP monitoring is recommend for admitted patients to help determine response to treatment
74
Management of CAP
Low-severity CAP:
5 days abx
1. amoxicillin is first-line
2. if penicillin allergic then use a macrolide or tetracycline
Moderate and high-severity CAP
1. dual antibiotic therapy is recommended with amoxicillin and a macrolide, a 7-10 day course is recommended
+ Consider a beta-lactamase stable penicillin such as co-amoxiclav, ceftriaxone or piperacillin with tazobactam and a macrolide in high-severity community acquired pneumonia
75
discharge criteria pneumonia
NICE recommend that patients are not routinely discharged if in the past 24 hours they have had 2 or more of the following findings:
temperature higher than 37.5°C
respiratory rate 24 breaths per minute or more
heart rate over 100 beats per minute
systolic blood pressure 90 mmHg or less
oxygen saturation under 90% on room air
abnormal mental status
inability to eat without assistance.
76
what should happen after 6 weeks following pneumonia
CXR
All cases of pneumonia should have a repeat chest X-ray at 6 weeks after clinical resolution to ensure that the consolidation has resolved and there is no underlying secondary abnormalities (e.g. a lung tumour).
77
most common causes pneumonia
Streptococcus pneumoniae (50%)
Haemophilus influenzae (20%)
Moraxella catarrhalis in immunocompromised patients or those with chronic pulmonary disease
Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis
Staphylococcus aureus in patients with cystic fibrosis
78
what organism may be causing pneumonia in immunocompromised or COPD patients
moxarella catarrhalis
79
what organisms may be causing pneumonia in CF/bronchiectasis
Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis
Staphylococcus aureus in patients with cystic fibrosis
80
what is the definiton of atypical pneumonia? What can they be treated with?
pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain.
They don’t respond to penicillins and can be treated with macrolides (e.g. clarithomycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline).
81
pneumonia caused by infected water supplies or air conditioning units. cheap holiday
Legionella pneumophila (Legionnaires’ disease)
82
how may legionnaires disease present
hyponatraemia (low sodium) by causing an SIADH
83
a mild penumonia causing erythema multiforme characterised by varying sized “target lesions” formed by pink rings with pale centres. It can also cause neurological symptoms in young patient
mycoplasma pneumoniae
84
pneumonia in a school aged child - chronic wheeze
Chlamydophila pneumoniae
other ddx more likely
85
pneumonia in a patient exposed to animals and their body fluids
Coxiella burnetii AKA “Q fever”
86
pneumonia in someone in contact with birds
Chlamydia psittaci
87
what are the 5 causes of atypical pneumonia
“Legions of psittaci MCQs”
Legions- legionella pneumophila
Psittaci - chlamydia psittaci
M – mycoplasma pneumoniae
C – chlamydydophila pneumoniae
Qs – Q fever (coxiella burnetii)
88
who may get fungal pneumonia? what is it called?
Pneumocystis jiroveci (PCP) pneumonia occurs in patients that are immunocompromised.
It is particularly important in patients with poorly controlled or new HIV with a low CD4 count. It usually presents subtly with a dry cough without sputum, shortness of breath on exertion and night sweats.
desaturation on exertion
89
management pneumocystitis jiroveci
co-trimoxazole (trimethoprim/sulfamethoxazole) known by the brand name “Septrin”
90
of the people exposed to TB, how many will develop it in their lifetime
5% get latent TB which becomes active a long time after infection
5% get active TB within 2 years
91
Typical history TB
Tuberculosis usually presents with a history of chronic, gradually worsening symptoms. Most cases are of pulmonary TB (around 70%) but they often have systemic symptoms.
Typical signs and symptoms of TB include:
Lethargy
Fever or night sweats
Weight loss
Cough with or without haemoptysis
Lymphadenopathy
Erythema nodosum
Spinal pain in spinal TB (also known as Pott’s disease of the spine)
92
what is the mantoux test for TB?
mantoux test - tuberculin skin prick - 5mm or more = positive
Positive in previous vaccination, latent TB or actvive TB
93
what is the quatiferon test for TB?
Interferon-Gamma Release Assays (IGRAs)
This test involves taking a sample of blood and mixing it with antigens from the TB bacteria. In a person that has had previous contact with TB the white blood cells have become sensitised to those antigens and they will release interferon-gamma as part of an immune response. If interferon-gamma is released from the white blood cells then this is considered a positive result.
positive in latent TB and active TB
think about pre-test probability before ordering this test
94
what is the gold standard invetsigation for active TB
Sputum culture.
Once cultured you can stain it (in same way as a smear) - more likely to be positive as has time to grow
more sensitive than a sputum smear and nucleic acid amplification tests
can assess drug sensitivities
can take 1-3 weeks (if using liquid media, longer if solid media)
If they are not producing sputum then hypertonic saline can be used to induce sputum that can be collected. They might require bronchoscopy with lavage to collect sputum samples.
Other cultures:
Mycobacterium blood cultures. These require special blood culture bottle.
Lymph node aspiration or biopsy
95
what is a sputum smear TB? results?
It is where a sputum sample is stained wither using ziel-neelson or phenoralamine - immunofluoresence test
3 specimens are needed
rapid and inexpensive test
stained for the presence of acid-fast bacilli (Ziehl-Neelsen stain)
all mycobacteria will stain positive (i.e. nontuberculous mycobacteria)
the sensitivity is between 50-80%
this is decreased in individuals with HIV to around 20-30%
96
what is a NAAT/PCR for TB?
allows rapid diagnosis (within 24-48 hours)
more sensitive than smear but less sensitive than culture
It provides information about the bacteria faster than a traditional culture but is only used where having this information would affect treatment or they are at higher risk of developing complications (i.e. in HIV).
97
how does primary TB present on CXR
patchy consolidation, pleural effusions and hilar lymphadenopathy
apical consolidation (top of lungs)
Development of tuberculous pleural effusion may occur as a result of delayed hypersensitivity reaction to mycobacteria or mycobacterial antigens in the pleural space in sensitized individuals [10] or by rupture of a subpleural focus of pulmonary disease into the pleural space
98
how does reactivated TB appear on CXR
upper lobe cavitation (gas filled spaces in the lungs) typically in the upper zones
99
how does miliary TB show on CXR
“millet seeds” uniformly distributed throughout the lung fields
100
most common site for TB infection?
lungs as get plenty O2
101
how may lymph node TB present
cold abscess” is a firm painless abscess caused by TB, usually in the neck. They do not have the inflammation, redness and pain you would expect from an acutely infected abscess.
102
where may you get granulomas TB
Pulmonary
Extrapulmonary:
lymph nodes
Pleura
Central nervous system
Pericardium
Gastrointestinal system
Genitourinary system
Bones and joints
Cutaneous TB affecting the skin
103
what is miliary TB
the immune system is unable to control the disease this causes a disseminated, severe disease
104
what type of vaccine is BCG
intradermal injection of live attenuated (weakened) TB
105
what must you do before BCG vaccine?
Prior to the vaccine patients are tested with the Mantoux test and given the vaccine only if this test is negative. They are also assessed for the possibility of immunosuppression and HIV due to the risks related to a live vaccine.
106
who is eligible for BCG vaccine?
Neonates born in areas of the UK with high rates of TB
Neonates with relatives from countries with a high rate of TB
Neonates with a family history of TB
Unvaccinated older children and young adults (< 35) who have close contact with TB
Unvaccinated children or young adults that recently arrived from a country with a high rate of TB
Healthcare workers
107
management latent TB
Otherwise healthy patients do not necessarily need treatment for latent TB. Patients at risk of reactivation of latent TB can be treated with either:
Isoniazid (with pyridoxine) and rifampicin for 3 months
(good for ppl under 35 if hepatotoxcity is a concern)
Isoniazid (with pyridoxine) for 6 months
(for ppl where rifampicin is a concern eg HIV or post transplant)
108
Management of active TB?
combination of 4 drugs used at the same time:
R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months
109
they are started on RIPE, what else should be prescribed?
pyridoxine (vitamin B6) is usually co-prescribed prophylactically to help prevent peripheral neuropathy from isoniazid
110
MoA and side effects rifampicin
"red and orange pissin"
hepatitis, organe secretions
inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA
111
MoA and side effects isoniazid?
"Im-so-numb-i-said"
peripheral neuropathy
hepatitis, orange secretions
agranulocytosis
inhibits mycolic acid synthesis
112
MoA and side effects pyrazinamide
hyperuricarmia causing gout
arhtalgia, myalgia
hepatitis
converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase (FAS) I
113
MoA and d=side effects ethambutol?
other considertaion
“eye-thambutol”
optic neuritis: check visual acuity before and during treatment
dose needs adjusting in patients with renal impairment
inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan
114
Fever pain score
Fever during previous 24 hours
P – Purulence (pus on tonsils)
A – Attended within 3 days of the onset of symptoms
I – Inflamed tonsils (severely inflamed)
N – No cough or coryza
A score of 2 – 3 gives a 34 – 40% probability (consider abx) and 4 – 5 gives a 62 – 65% probability of bacterial tonsillitis (give abx)
115
Management tonsilitis
1. Oral phenoxymethylpenicillin (penicillin V?) for 5 or 10 days
2. Clarithomycin or erythromycin(if penicillin allergic)5 days
116
Chronic tonsilitis referral criteria
>3 episodes per year for 3 years
>5 episodes per year for two years
>7 episodes in a single year
Refer to ENT for tonsillectomy
117
Pathogen bacterial tonsilitis
GABS Group A Beta-haemolytic streptococcus
118
Two most common bacterial causes of otitis externa?
- pseudomonas aerginosa
- staphlococcus aureus
119
management of otitis externa
mild
1. acetic acid drops 2%
moderate: unclear if this is norm 1st line instead of above..
1. Topical abtibiotic and steroid eg:
Otomize spray (Neomycin, dexamethasone and acetic acid)
2. orla fluclox if spreading
Fungal:
1. Clotrimazole ear drops
120
Most common pathogen and others : otitis media
Streptococcus pneumoniae
Other common causes include:
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
121
If giving abx for otitis media, what is first line? what are alterantives?
1. amoxicillin for 5 days
alternatives: erythromycin or clarythromycin
122
Management fungal otitis externa
clotrimazole ear drops
123
What should be avoided if perforated ear drum
Aminoglycosides (e.g., gentamicin and neomycin) are potentially ototoxic, rarely causing hearing loss if they get past the tympanic membrane.
124
Complication of otitis externa?
malignant otitis externa
Admission to hospital under the ENT team
IV antibiotics
Imaging (e.g., CT or MRI head) to assess the extent of the infection
125
pathophysiology otitis media
whilst viral upper respiratory tract infections (URTIs) typically precede otitis media, most infections are secondary to bacteria, particularly Streptococcus pneumonaie, Haemophilus influenzae and Moraxella catarrhalis
viral URTIs are thought to disturb the normal nasopharyngeal microbiome, allowing bacteria to infect the middle ear via the Eustachian tube
126
Presentation otitis media
otalgia
+ some children may tug or rub their ear
fever occurs in around 50% of cases
hearing loss
recent viral URTI symptoms are common (e.g. coryza)
ear discharge may occur if the tympanic membrane perforates
127
Examination otitis media
bulging tympanic membrane → loss of light reflex
opacification or erythema of the tympanic membrane
perforation with purulent otorrhoea
decreased mobility if using a pneumatic otoscope
128
Who should get antibiotics for otitis media
Features:
Symptoms lasting more than 4 days or not improving
Systemically unwell but not requiring admission
Otitis media with perforation and/or discharge in the canal
Patient:
Immunocompromised or high risk of complications secondary to significant heart, lung, kidney, liver, or neuromuscular disease
Younger than 2 years with bilateral otitis media
129
complications otitis media
Otitis media with effusion
Hearing loss (usually temporary)
Perforated eardrum
Recurrent infection
Mastoiditis (rare)
Abscess (rare)
130
what is mastoiditis ? cause? typical presentation?
Mastoiditis typically develops when an infection spreads from the middle to the mastoid air spaces of the temporal bone.
PC:
otalgia: severe, classically behind the ear
there may be a history of recurrent otitis media
fever
the patient is typically very unwell
swelling, erythema and tenderness over the mastoid process
the external ear may protrude forwards
ear discharge may be present if the eardrum has perforated
131
management mastoiditis? complications?
The diagnosis is typically clinical although a CT may be ordered complications are suspected.
Management
IV antibiotics
Complications
facial nerve palsy
hearing loss
meningitis
132
how does viral URTI precede bacterial otitis media??
viral URTIs are thought to disturb the normal nasopharyngeal microbiome, allowing bacteria to infect the middle ear via the Eustachian tube
133
history and exam otitis externa
The typical symptoms of otitis externa are:
Ear pain
Discharge
Itchiness
Conductive hearing loss (if the ear becomes blocked)
Examination can show:
Otoscopy: red, swollen, or eczematous canal
Erythema and swelling in the ear canal
Tenderness of the ear canal
Pus or discharge in the ear canal
Lymphadenopathy (swollen lymph nodes) in the neck or around the ear
134
what is infectious mononucleosis also called? cause?
(Glandular fever)
Epstein-Barr virus (EBV, also known as human herpesvirus 4, HHV-4) in 90% of cases
Less frequent causes include cytomegalovirus and HHV-6
135
typical history EBV - triad?
- sore throat
- lymphadenopathy
- pyrexia
Other features:
malaise, anorexia, headache
palatal petechiae
splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture
hepatitis, transient rise in ALT
lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes
haemolytic anaemia secondary to cold agglutins (IgM)
a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
136
lymphadenopathy EBV vs tonsilitis
in EBV may be present in the anterior and posterior triangles of the neck, in contrast to tonsillitis which typically only results in the upper anterior cervical chain being enlarged
137
investigation glandular fever?
heterophil antibody test (Monospot test)
NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever.
138
management EBV
rest during the early stages, drink plenty of fluid, avoid alcohol
simple analgesia for any aches or pains
consensus guidance in the UK is to avoid playing contact sports for 4 weeks after having glandular fever to reduce the risk of splenic rupture
139
steady non-paroxysmal pain in epigastrium/RUQ that radiates to back PLUS fever and tenderness
acute cholecystitis
140
o/e acute cholecystitis
fever
tenderness
murphys sign positive
no jaundice
141
Plan acute cholecystitis
Investigations:
Carried out in hospital
- abdominal USS
- Bloods (raised WCC, raised CRP, serum amylase)
Management:
Admit to hospital
Analgesia
Monitoring
IV fluids
Antibiotics
Surgical assessment for cholecystectomy (to be done within 1 week of presentation, ideally within 48 hours)
142
What is mirizzi syndrome
A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct.
This results in an obstructive jaundice, even without stones being present within the lumen of the common hepatic or common bile ducts.
Investigation:
MRCP
Management:
Laparoscopic cholecystectomy
143
What is chronic cholecystitis
PC: recurrent or untreated acute cholecystitis —> persistent inflammation of gallbladder wall
Management:
Elective cholecystectomy
144
What is gallbladder empyema
Gallbladder fills with pus and patient may become septic
PC: similar to acute cholecystitis
145
Pathophysiology ascending cholangitis
Infection of biliary tract caused by biliary outflow obstruction and biliary infection. Stasis of fluid allows bacterial colonisation.
Main organisms are: e.coli, klebsiella and enterococcus
146
fever, jaundice, RUQ pain
charcots triad - indicates ascending cholangitis
147
typical history ascending cholangitis
PC: fever, jaundice, RUQ pain (charcots triad)
HoPC: may have pyrexia, rigours, jaundice, RUQ tenderness, confusion, hypotension, tachycardia
Red flags:
Environment:
MHx: gallstones, recent ERCP procedure, previous cholangitis
DHx: oral contraceptive pill and fibrates
FHx:
SHx: diet rich in fatty foods
148
Plan ?ascending cholangitis
Initial management:
IV access
Fluid resuscitation
Antibiotics broad spectrum eg co-amoxiclav +metronidazole
Investigation/management:
blood cultures
ERCP with or without sphincterotomy and stunting
Long term may require cholecystectomy of gallstones were the cause
149
o/e ascending cholangitis
fever
tenderness
jaundice
confusion
hypotension
tachycardia
150
what is peritonitis? what are the signs on examination?
Peritonitis refers to inflammation of the peritoneum, the lining of the abdomen. The signs of peritonitis are:
Guarding – involuntary tensing of the abdominal wall muscles when palpated to protect the painful area below
Rigidity – involuntary persistent tightness / tensing of the abdominal wall muscles
Rebound tenderness – rapidly releasing pressure on the abdomen creates worse pain than the pressure itself
Coughing test – asking the patient to cough to see if it results in pain in the abdomen
Percussion tenderness – pain and tenderness when percussing the abdomen
151
what us localised peritonitis ? what does it indicate?
Localised peritonitis is caused by underlying organ inflammation, for example, appendicitis or cholecystitis.
152
what is generalised peritonitis? what does it indicate?
Generalised peritonitis may be caused by perforation of an abdominal organ (e.g., perforated duodenal ulcer or ruptured appendix) releasing the contents into the peritoneal cavity and causing generalised inflammation of the peritoneum.
153
what is spontaneous bacterial peritonitis
Spontaneous bacterial peritonitis is associated with spontaneous infection of ascites in patients with liver disease. This is treated with broad-spectrum antibiotics and carries a poor prognosis.
154
plan ?peritonitis
peritonitis is a cause of 'acute abdomen'
start with ABCDE, wide scope of investigation and prompt management - see 'acute abdomen'
management involves IV abx and emergency surgery
155
plan ?spontanous bacterial peritonitis
Investigation
paracentesis: neutrophil count > 250 cells/ul
the most common organism found on ascitic fluid culture is E. coli
Management
intravenous cefotaxime is usually given
156
typical history SBP
ascites
abdominal pain
fever
157
who should get prophylaxic abx if they have ascites?
patients who have had an episode of SBP
patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
NICE recommend: 'Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved'
158
what is gastroenteritis
Gastroenteritis is a transient disorder due to enteric infection, usually caused by viruses, characterised by sudden onset of diarrhoea, with or without vomiting.
159
what is dysentery
Dysentery is an infection of the intestines that causes diarrhoea containing blood or mucus.
160
define acute diarrhoea
3 or more episodes of liquid or semi-liquid stool in a 24-hour period,
lasting for less than 14 days, where the stool takes the shape of the sample pot.
161
define prolonged diarrhoea
acute-onset diarrhoea that has persisted for over 14 days.
162
complications of gastroenteritis
dehydration, electrolyte disturbance, acute kidney injury, sepsis, haemolytic uraemic syndrome, and secondary irritable syndrome or inflammatory bowel syndrome.
163
Approach to gastroenteritis
Assess for signs of dehydration, sepsis, shock (SEE DEHYDRATION AND SHOCK)
1. Arrange hospital admission if sys unwell/sepsis/severe dehydration/child with ? or confirmed STEC/?HUS
2. Arrange for stool culture and sensitivity if indicated
sys unwell/dysentry/recent abx or PPI (to exclude c.diff)/diarrhoea not resolved by day 7/?food poisoning/recent travel/someone at risk of transmission/asymp been in contact with risky contacts eg confirmed STEC or giardia
3. Send additional 3 samples 2-3 days apart for ova, cysts and parasites if recent travel or symptoms >14 days
4. Hydration, ORS if at risk
5. advise abx or antimotility or antiemetics and probiotics not routinely reccomended
6. Advise measures to prevent transmission eg hygeine, 60 degrees, 48 hours symptom free before return to work
7. Notify PH fir food poisoning, HUS, infectious bloody diarrhoea, enteric fever, cholera
164
most common cause gastroenteritis
viral
rotavirus in children (immunnity long lasting)
norovirus in adults (immunity short lasting)
165
typical history norovirus
Sudden-onset nausea is followed by projectile vomiting and watery diarrhoea. There may be associated fever, headache, abdominal pain, and myalgia.
Most people make a full recovery within 1–2 days.
Symptoms begin 24–48 hours after infection and last for 12–60 hours.
166
causes of travellers diarrhoea
e.coli most common
campylobacter jej
167
gastroenteritis causes incubation period 1-6 hrs
staph aureus
bacillus cereus
168
gastroenteritis causes incubation period 12-48 hrs
salmonella
e.coli
169
gastroenteritis causes incubation period 48-72 hours
shigella
camylobacter
170
gastroenteritis causes incubation period >7days
giardiasis
amobiasis
171
what gastroenteritises may cause dysentery
e.coli 0157
shigella
amobieasis
172
management campylobacter jejuni
almost always supportive
however if symptoms are severe (high fever, bloody and/or high-output diarrhoea) or the person is immunocompromised, consider early prescribing with clarithromycin 250–500 mg twice daily for 5–7 days, within 3 days of onset of illness
173
management e.coli
Illness is usually self-limiting and resolves within 10 days
seek specialist advice for:
- whether stool testing for clearance is required
- monitoring for HUS
174
typical history staph aureus gastroenteritis
Short incubation period eg 6 hours, severe vomiting
175
typical history bacillus cereus
vomiting within 6 hours, stereotypically due to rice
diarrhoeal illness occurring after 6 hours
176
typical history campylobacter jejuni
PC: abdo cramps, diarrhoea often with blood, vomiting, fever, flu-like prodrome
Incubation 2-5 days, symptoms resolve after 3-6 days
Risk factors: travel, undercooked meat (particularly poultry), unpasteurised milk, untreated water. Source often not found
177
what type of pathogen is e.coli, gram etc
facultative anaerobic, lactose-fermenting, Gram negative bacilli
178
typical history e.coli
PC: Watery stools with or without blood, abdominal cramps, nausea, fever.
Illness is usually self-limiting and resolves within 10 days.
Risk factors: travel, contact with faeces, unwashed salad, contaminated meat
179
typical history salmonella
PC: watery and sometimes bloody diarrhoea, abdominal pain, headache, nausea, vomiting, and fever. The illness usually lasts for 4–7 days, and people usually recover spontaneously.
The majority of cases are sporadic, but outbreaks may occur in the general population and in institutions.
Ingestion of contaminated food is the most common source, such as red and white meats, raw eggs, milk, and dairy products. Person-to-person spread and contact with infected animals can also occur.
180
typical history shigella
Typically, 1–3 days after infection, there is diarrhoea (may have blood and mucus), fever, and abdominal cramps, with or without nausea and vomiting, headache, and malaise. Shigellosis usually resolves in 5–7 days.
181
management shigella
Antibiotic treatment is not usually needed for people with mild symptoms.
If symptoms are severe (high fever, bloody and/or high-output diarrhoea) or the person is immunocompromised, seek specialist advice on the need for antibiotic treatment.
182
typical history yersinia enterocolitica
rare infection and occurs most commonly in children.
PC: watery diarrhoea (which is often bloody), fever, and abdominal pain. In older children and adults, right-sided abdominal pain and fever may occur.
Symptoms typically develop 4–7 days after exposure and may last 2 days to 6 weeks.
Y. enterocolitica is transmitted by direct contact with infected animals and person-to-person (faecal-oral route), and through contaminated food (especially raw pork and pork products) and water.
183
typical history cryptosporidiosis
PC: profuse watery diarrhoea associated with abdominal cramps or pain, nausea, vomiting, fever, and loss of appetite. Symptoms usually last for 1–2 weeks, and recurrence of symptoms is reported in around one-third of cases.
risk: recent travel, water, food
184
typical history amoebiasis
PC: mild diarrhoea and abdominal pain, but severe disease (amoebic dysentery) can occur, causing fever, severe abdominal pain, and blood and mucus in the faeces.
185
management amoebiasis
Seek specialist advice:
1. metronidazole followed by the anti-protozoal drug diloxanide. (to eliminate intraluminal cysts)
Seek specialist advice regarding the need for microbiological clearance to confirm treatment success, 1 week after completing treatment.
186
complication of amoebic gastroenteritis? management?
Amoebic liver abscess
usually a single mass in the right lobe (may be multiple). The contents are often described as 'anchovy sauce'
features
fever
right upper quadrant pain
systemic symptoms e.g. malaise
hepatomegaly
investigations
ultrasound
serology is positive in > 95%
management
oral metronidazole
a 'luminal agent' (to eliminate intraluminal cysts) is recommended usually as well e.g. diloxanide furoate
187
typical history giardia
prolonged diarrhoea, malaise, abdominal pain, loss of appetite, flatulence, bloating, and rarely nausea. Malabsorption, weight loss, and faltering growth may occur in children
188
management giardia
tinidazole 2 g as a single dose
189
Complication of e.coli and shigella
haemolytic uraemic syndrome?
190
typical history HUS? triad?
PC: brief gastroenteritis, bloody diarrhoea. 5 days after : decreased urine output, hematuria, abdo pain, lethargy, bruising, hematuria, confusion, hypertension
Triad: haemolytic anaemia, acute kidney injury, thrombocytopenia
191
why are antibiotics and antimotility agents not recommended in gastroenteritis
if has shiga toxin producing pathogen --> increases risk of HUS
192
management HUS
HUS is a medical emergency and has up to 10% mortality
Supportive
Antihypertensives
Blood transfusion
Hemodialysis
193
what is a cause of pneumonia particualrly in COPD
haemophilus influenzae
194
what pneumonia is common after infleunza?
staph aureus
195
what pneumonia is comon in patients with high alcohol consumption
klebisella pneumoniae
196
typical causes of hospital acquired penumonia (HAP)
pseudomonas aeruginosa, e.coli, klebsiella pneumoniae, acinetobacter species
197
management HAP
Mild/moderate symptoms and not at higher risk of resistance :
consider amoxicillin
Severe symptoms and at higher risk of resistance :
1. IV broad spectrum abx (eg pip taz, ceftazidime, ceftriaxone, cefuroxime, meropenem, ceftazidime/avibactam, levofloxacin)
+ In patients with suspected or confirmed MRSA add IV vancomycin or teiciplanin
Review all patients within 48 hours and if possible switch to oral
198
peak incidence of appendicitis
patients aged 10-20 years
199
pathophysiology appendicitis
There is a single opening to the appendix that connects it to the bowel, and it leads to a dead end.
Pathogens can get trapped due to obstruction at the point where the appendix meets the bowel. Trapping of pathogens leads to infection and inflammation. The inflammation may proceed to gangrene and rupture. When the appendix ruptures, faecal contents and infective material are released into the peritoneal cavity. This leads to peritonitis, which is inflammation of the peritoneal lining.
200
typical history and exam appendicitis
PC: abdominal pain, starts central and then localises to right iliac fossa within first 24 hours, anorexia (loss of appetitie), N&V, low grade fever,
o/e:
- tenderness at McBurney's point (one third of the distance from the anterior superior iliac spine (ASIS) to the umbilicus. )
- Rovsing’s sign (palpation in LIF → causes pain in RIF)
signs of peritonitis which may indicate ruptured appendix : general pain indicates rupture where as localised is reassuring
- Rebound tenderness (increased pain when suddenly releasing the pressure of deep palpation
- Percussion tenderness
- guarding
- coughing test
201
plan ?appendicitis
ABCDE approach
part of 'acute abdomen'
Diagnosis is mostly clinical
1. Clinical presentation + raised inflammatory markers
+ CT useful in confirming particularly where another diagnosis is more likely
+ USS is often used in female patients to exclude gynae pathology
2. Diagnostic laparoscopy → appendectomy if appendicitis
202
when is CT useful ?appendicitis
where another diagnosis is more likely
203
when is USS useful ?appendicitis
in female patients to exclude gynae pathology
preferred imaging modality in children, pregnant, and breastfeeding women
204
when would an MRI be used ?appendicitis
MRI scans are mainly reserved for pregnant women when ultrasound is non-diagnostic
205
complications of appendectomy
Bleeding, infection, pain and scars
Damage to bowel, bladder or other organs
Removal of a normal appendix
Anaesthetic risks
Venous thromboembolism (deep vein thrombosis or pulmonary embolism)
206
What is a diverticulum
A diverticulum (plural diverticula) is a pouch or pocket in the bowel wall, usually ranging in size from 0.5 – 1 cm.
Diverticula are sac-like protrusions of mucosa through the muscular wall of the colon, which occur in the sigmoid colon in about 80% of people over the age of 85.
(like mini hernias)
207
What is diverticulosis
Diverticulosis refers to the presence of diverticula, without inflammation or infection.
Diverticulosis may be referred to as diverticular disease when patients experience symptoms.
208
what is diverticulitis
Diverticulitis refers to inflammation and infection of diverticula.
209
why don't you get diverticula in rectum
Diverticula do not form in the rectum, because it has an outer longitudinal muscle layer that completely surrounds the diameter of the rectum, adding extra support.
In the rest of the colon, there are three longitudinal muscles that run along the colon, forming strips or ribbons called teniae coli. The teniae coli do not surround the entire diameter of the colon, and the areas that are not covered by teniae coli are vulnerable to the development of diverticula.
210
risk factors diverticulosis
increased age, low fibre diets, obesity and the use of NSAIDs are risk factors.
211
Presentation diverticulosis
Often diagnosed incidentally on colonoscopy or CT scans.
Diverticulosis may cause lower left abdominal pain, constipation or large painless rectal bleed.
212
plan ?diverticulosis or confirmed diverticulosis
management
- Not necessary where the patient is asymptomatic. However, advice regarding a high fibre diet and weight loss is appropriate.
- If symptomatic increased fibre in the diet and bulk-forming laxatives (e.g., ispaghula husk).
- Surgery to remove the affected area may be required where there are significant symptoms.
213
what medications should be avoided in diverticualr disease
Stimulant laxatives (e.g., Senna)
NSAIDS - increases risk of hemorrhage
Opiod analgesia
214
Typical history acute diverticulitis
Pain and tenderness in the left iliac fossa / lower left abdomen
Fever
Diarrhoea
Nausea and vomiting
Rectal bleeding
check for signs of complicated:
Palpable abdominal mass (if an abscess has formed)
Peritonitis
215
what is uncomplicated diverticulitis
Refers to diverticular inflammation that does not extend to the peritoneum.
216
what is complicated diverticulitis? when to suspect?
'Complicated' diverticulitis refers to diverticulitis associated with complications, such as abscess, peritonitis, fistula, obstruction, or perforation.
Suspect a complication of diverticulitis if the person has uncontrolled abdominal pain and any of the following features:
- Abdominal mass on examination or peri-rectal fullness on digital rectal examination — possible intra-abdominal abscess.
- Abdominal rigidity, guarding, and rebound tenderness on examination — possible perforation and peritonitis.
- Altered mental state, raised respiratory rate, low systolic blood pressure, raised heart rate, low tympanic temperature, no urine output or skin discolouration — possible sepsis.
- Faecaluria, pneumaturia, pyuria or passage of faeces through the vagina — possible colovesical fistula.
- Colicky abdominal pain, absolute constipation (passage of no flatus or stool), vomiting or abdominal distention — intestinal obstruction.
217
management of uncomplicated diverticulitis
- Oral co-amoxiclav (at least 5 days)
- Analgesia (avoiding NSAIDs and opiates, if possible)
- Only taking clear liquids (avoiding solid food) until symptoms improve (usually 2-3 days)
- Follow-up within 2 days to review symptoms, if still present/not improving, admit for IV abx
218
plan ?complicated diverticulitis
treat as acute abdomen and specific to complication eg sepsis etc
Investigations if admitted:
FBC: raised WCC
CRP: raised
Erect CXR: may show pneumoperitoneum in cases of perforation
AXR: may show dilated bowel loops, obstruction or abscesses
CT: this is the best modality in suspected abscesses
Colonoscopy: should be avoided initially due to the increased risk of perforation in diverticulitis
Management
Nil by mouth or clear fluids only
IV antibiotics
IV fluids
Analgesia
Urgent investigations (e.g., CT scan)
Urgent surgery may be required for complications
219
Complications of acute diverticulitis
Perforation
Peritonitis
Peridiverticular abscess
Large haemorrhage requiring blood transfusions
Fistula (e.g., between the colon and the bladder or vagina)
Ileus / obstruction
220
Typical history meningitis
Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures
Non-blanching rash
Neonates:
Hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle.
Therefore lumbar puncture in all children if:
Under 1 month old and presenting with fever
1-3 months with fever and unwell
Under 1 years with unexplained fever and other features of serious illness
221
Examination findings meningitis
Fever
Non-blanching rash
Photophobia
Kernig's test (Kernig’s test involves lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges and where there is meningitis will produce spinal pain or resistance to this movement.)
Brudzinski test (Brudzinski’s test involves lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. A positive test is when this causes the patient to involuntarily flex their hips and knees.)
222
What is Meningococcal meningitis vs Meningococcal septicaemia
Meningococcal meningitis - meningococcus bacteria (neisseria meningitidis) is infecting the meninges and CSF
Meningococcal septicaemia - meningococcal bacterial infection in the bloodstream → non blanching rash due to DIC and subcutaneous haemorrhage
223
plan ?meningitis
Airway
Breathing
Circulation
Disability: GCS, ; focal neurological signs; seizures; papilloedema;
Initial:
if in primary care and ?meningococcal - an urgent stat injection (IM or IV) of benzylpenicillin prior to transfer to hospital as time is so important:
< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg
Once in hospital, decisions to treat empirically quickly vs LP depends on patient and senior clinician
Investigations:
Bloods:
- full blood count
- CRP
- coagulation screen
Blood culture
Whole-blood PCR, this will be relied upon if lumbar puncture contraindicated
Blood glucose
Blood gas
Throat and nose swabs (cultured and PCR for viruses)
Stool PCR for enterovirus
Lumbar puncture
unless contraindicated eg if there is evidence of raised ICP as it can cause herniation of cerebrum. Signs of raised ICP: cushing's reflex (raised BP, low HR), focal neurological signs, papilloedema, significant bulging of the fontanelle, disseminated intravascular coagulation (meningococcal septicaemia eg the rash), signs of cerebral herniation.
Blood glucose at same time as CSF so can be compared
224
Normal lumbar puncture result
clear appearance
glucose 70% of plasma
protein 0.3 g/l
WCC 2 per mm^3 (neuts)
225
Bacterial meningitis LP result
Cloudy
Glucose low (< 1/2 plasma) bacteria using up the glucose
Protein high (> 1 g/l) bacteria releasing proteins
WCC 10 - 5,000 polymorphs/mm³ the immune system releases neutrophils in response to bacteria
226
Viral meningitis LP result
Clear/cloudy
Glucose 60-80% of plasma glucose* viruses don’t really use glucose
Protein normal/raised viruses may release a small amount of protein
WCC 15 - 1,000 lymphocytes/mm³ the immune system releases lymphocytes in response to viruses
227
Tuberculous LP result
Slight cloudy, fibrin web
glucose Low (< 1/2 plasma)
Protein high >1g/l
WCC 30-300 lymphocytes/mm3
The Ziehl-Neelsen stain is only 20% sensitive in the detection of tuberculous meningitis and therefore PCR is sometimes used (sensitivity = 75%)
228
Bacterial meningitis 0-3 months
BELS
1. Group B Streptococcus (most common cause in neonates)
2. E. coli
3. Listeria monocytogenes
4. Strep pneumoniae
229
Bacterial meningitis 3 months-6 years
1. Neisseria meningitidis
2. Streptococcus pneumoniae
3. Haemophilus influenzae
230
Bacterial meningitis 6-60 years
1. Neisseria meningitidis
2. Streptococcus pneumoniae
231
Bacterial meningitis >60 years
1. Streptococcus pneumoniae
2. Neisseria meningitidis
3. Listeria monocytogenes
232
Meningitis in immunocompromised
listeria monocytogenes
233
Community meningitis initial management
Benzylpenicillin IM or IV
< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg
234
Meningitis initial empirical therapy < 3 months
IV cefotaxime + amoxicillin (or ampicillin)
235
Meningitis initial empirical therapy 3 months-50 years
IV cefotaxime
236
Meningitis initial empirical therapy > 50 years
IV cefotaxime + amoxicillin (or ampicillin)
237
Meningitis management - listeria
IV amoxicillin (or ampicillin)
+ gentamicin
238
When should dexamethasone be given for meningitis
Give if lumbar puncture reveals:
- frankly purulent CSF
-CSF white blood cell count greater than 1000/microlitre
- raised CSF white blood cell count with protein concentration greater than 1 g/litre
- bacteria on Gram stain
Withhold if:
- septic shock
- meningococcal
- septicaemia
immunocompromised
dexamethasone is only useful for pneumococcal. start in everyone unless CI and then change later
239
Management meningococcal meningitis
IV benzylpenicillin or cefotaxime
240
Post exposure prophylaxis bacterial meningitis
Ciprofloxacin single dose
This risk is highest for people that have had close prolonged contact within the 7 days prior to the onset of the illness
241
Typical history encephalitis
PC:
Fever
Headache
Confusion
- psychiatric symptoms
- vomiting
- seizures
- focal features
242
Brain scan where does encephalitis classically affect
temporal lobe
243
Most common pathogen encephalitis in children and adults
herpes simplex HSV-1 from cold sores
other:
Varicella zoster virus
Parvoviruses
HIV
Mumps virus
Measles virus
244
Most common pathogen encephalitis in neonates
herpes simplex type 2 (HSV-2) from genital herpes, contracted during birth.
think "been passed on 2"
245
Plan ?encephalitis
Initial:
Immediate IV aciclovir (covers HSV and varicella zoster)
Invetsigations:
- CSF : lymphocytosis, raised protein
- PCR for HSV
- CT medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients.
- MRI is better
- EEG pattern: lateralised periodic discharges at 2 Hz
246
Management CMV encephalitis
Ganciclovir
247
Typical history brain abscess
PC:
- dull persistant headache
- fever
- focal neurology
- features of raised ICP
248
Plan ?brain abscess
Invetsigation:
- CT
- invetsigate for sepsis and ddx etc
Management:
1. surgery
a craniotomy is performed and the abscess cavity debrided
the abscess may reform because the head is closed following abscess drainage.
1. IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
1. intracranial pressure management: e.g. dexamethasone
249
most common causes viral meningitis
echovirus, coxsackievirus
others:
Herpes simplex virus
Mumps virus
Lymphocytic chorio meningitis virus
And historically, Poliovirus (also an enterovirus)
250
management viral meningitis
supportive,
if HSV suspected - aciclovir
251
Complications of meningitis
Hearing loss
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Focal neurological deficits such as limb weakness or spasticity
252
what are the most commonly affected joints septic arthritis
hip, knee and ankle
253
typical history septic arthritis
PC: hot red swollen painful joint, stiffness and reduced range of motion, systemic symptoms such as fever and lethargy
any hot/red joint
254
most common causative organism septic arthritis ? other causes
staph aureus
Neisseria gonorrhoea (gonococcus) in sexually active teenagers
Group A streptococcus (Streptococcus pyogenes)
Haemophilus influenza
Escherichia coli (E. coli)
255
young pt presenting with single acutely swollen joint - first ddx?
always think of gonococcus septic arthritis until proven otherwise
Gonorrhoea infection is common and delaying treatment puts the joint in danger. In your exams it might say the gram stain revealed a “gram-negative diplococcus”. The patient may have urinary or genital symptoms to trick you into thinking of reactive arthritis but remember that it is important to exclude gonococcal septic arthritis first as this is the more serious condition.
256
plan ?septic arthritis
Have a low suspicion until joint fluid assessed
1. Aspiration for gram stain, crystal microscopy, culture and antibiotic sensitivities
2. If paeds, USS, if shows effusion and with corroborating history, treat as septic arthritis
3. Bloods inflammatory markers, blood culture
4. Empirical IV antibiotics (local guidelines)
5. Continue abx for 3-6 weeks
Patients may require surgical drainage and washout of the joint to clear the infection in severe cases.
257
example first line regime septic arthritis abx
Flucloxacillin for 6 weeks
if pen allergic: clindamycin
If MRSA suspected: vancomycin
If gonococcal arthritis or gram -ve susepcted : cefotaxime or ceftriaxone
258
what criteria can be used in children to distinguish between septic arthritis and transient synovitis of hip
The kocher criteria
fever >38.5 degrees C
non-weight bearing
raised ESR > 40
raised WCC >12
If 0 = very unlikely and can be managed in primary care with close follow up
259
what is osteomyelitis
an infection in the bone and bone marrow.
This typically occurs in the metaphysis of the long bones.
260
what is the most common causative organism osteomyelitis
staph aureus
261
types of osteomyelitis and how do people get it?
Chronic osteomyelitis is a deep seated, slow growing infection with slowly developing symptoms.
Acute osteomyelitis presents more quickly with an acutely unwell pt.
The infection may be introduced directly into the bone, for example during an open fracture.
Alternatively it may have travelled to the bone through the blood, after entering the body through another route, such as the skin or gums.
262
In what children is osteomyelitis more common
boys and children under 10 years
263
typical history osteomyelitis
Osteomyelitis can present acutely with an unwell child, or more chronically with subtle features. Signs and symptoms are:
- Refusing to use the limb or weight bear
- Pain
- Swelling
- Tenderness
They may be afebrile, or may have a low grade fever. Children with acute osteomyelitis may have a high fever, particularly if it has spread to the joint causing septic arthritis.
264
best imaging for dx of osteomyelitis
MRI
265
initial invetsigation osteomyelitis
xray
266
plan investigation ?osteomyelitis
1. xray
2. MRI if xray inconclusive
3. inflammatory markers CRP, ESR, WCC
4. blood culture
267
management osteomyelitis
Osteomyelitis is treated with antibiotics, usually with surgical debridement
Flucloxacillin for 6 weeks
+ consider fusidic acid or rifmapicin
if pen allergic: clindamycin
If MRSA suspected: vancomycin
268
what is discitis
Discitis is an infection in the intervertebral disc space. It can lead to serious complications such as sepsis or an epidural abscess.
269
typical history discitis
Back pain
General features
pyrexia,
rigors
sepsis
Neurological features e.g. changing lower limb neurology if an epidural abscess develops
270
most common cause discitis
staph aureus
271
plan ?discitis
Invetsigation
Imaging: MRI has the highest sensitivity
blood culture
CT-guided biopsy may be required to guide antimicrobial treatment
transoesophageal/transthoracic echo to assess for endocarditis (seeding)
management
abx based on cultures/biopsy
272
define reactive arhtitis
An arthritis that develops following an infection where the organism cannot be recovered from the joint.
273
classic triad of reative arhtitis
'Can't see, pee or climb a tree'
conjunctivitis , urethritis and arthritis
274
most common caustive organism post sti reative arthritis
Chlamydia trachomatis
275
causative organisms post dysenteric reative arhtitis
Shigella flexneri
Salmonella typhimurium
Salmonella enteritidis
Yersinia enterocolitica
Campylobacter
276
management of reactive arthritis
symptomatic: analgesia, NSAIDS, intra-articular steroids
sulfasalazine and methotrexate are sometimes used for persistent disease
symptoms rarely last more than 12 months
277
Typical history infective endocarditis
PC:
Fever
Fatigue
Night sweats
Muscle aches
Anorexia (loss of appetite)
abdominal or chest pain
o/e:
New or “changing” heart murmur
Splinter haemorrhages
Petechiae on the trunk, limbs, oral mucosa or conjunctiva
Janeway lesions
Osler’s nodes
Roth spots
Splenomegaly (in longstanding disease)
Finger clubbing (in longstanding disease)
278
risk factors infective endocarditis
Intravenous drug use
Structural heart pathology (see below)
Chronic kidney disease (particularly on dialysis)
Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
History of infective endocarditis
279
define infetcive endocarditis
Infective endocarditis refers to infection of the endothelium (the inner surface) of the heart.
Most commonly, it affects the heart valves.
It can be acute, subacute or chronic, depending on how rapidly and acutely the symptoms present and the causative organism.
280
Examples of structural heart pathology that can increase risk of infetcive endocarditis
Valvular heart disease
Congenital heart disease
Hypertrophic cardiomyopathy
Prosthetic heart valves
Implantable cardiac devices (e.g., pacemakers)
281
most common causative oragnism infective endocarditis? other causes
Staphylococcus aureus
Other causes include:
Streptococcus (notably the viridans group of streptococci)
Enterococcus (e.g., Enterococcus faecalis)
Rarer causes include Pseudomonas, HACEK organisms and fungi
282
Invetsigations ?infective endocarditis
1. Three blood cultures, separated by 6 hours, taken from different sites (most important)
2. Echo (trans-oesohageal ideal but trans-thoracic done mostly)
283
what scans can be done if prosthetic heat valve ?infective endocarditis
18F-FDG PET/CT
SPECT-CT
284
What criteria is used for diagnosis of infective endocarditis
modified duke criteria
285
what is the modified duke criteria
The Modified Duke criteria can be used to diagnose infective endocarditis. A diagnosis requires either:
- One major plus three minor criteria
- Five minor criteria
Major criteria are:
- Persistently positive blood cultures (typical bacteria on multiple cultures)
- Specific imaging findings (e.g., a vegetation seen on the echocardiogram)
Minor criteria are:
- Predisposition (e.g., IV drug use or heart valve pathology)
- Fever above 38°C
- Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions)
- Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis)
- Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)
286
Management infective endocarditis
Intravenous broad-spectrum antibiotics (e.g., amoxicillin and optional gentamicin) are the mainstay of treatment.
The choice of antibiotic may be more specific once the causative organism is identified on cultures.
Antibiotics are typically continued for at least:
4 weeks for with native heart valves
6 weeks for patients with prosthetic heart valves
Surgery may be required for:
- Heart failure relating to valve pathology
- Large vegetations or abscesses
- Infections not responding to antibiotics
287
Complications of infective endocarditis?
- Heart valve damage, causing regurgitation
- Heart failure
- Infective and non-infective emboli (causing abscesses, strokes and splenic infarction)
- Glomerulonephritis, causing renal impairment
288
when is prophylaxis for infective endocarditis given
case by case basis for surgical procedures etc for those at particularly high risk
289
infective endocarditis poor oral hygeine/dental work
streptococcus viridians such as streptococcus mutans
290
infective endocarditis immunocompromise
candida albicans
291
infective endocarditis prosthetic valve (within 2 months)
staph epidermidis
292
infective endocarditis IVDU
s.aureus
293
infective endocarditis prostatitis
enterococcus faecalis
294
typical history PID
Pelvic or lower abdominal pain
Abnormal vaginal discharge
Abnormal bleeding (intermenstrual or postcoital)
Pain during sex (dyspareunia)
Fever
Dysuria
295
What is pelvic inflammatory disease
inflammation and infection of the organs of the pelvis, caused by infection spreading up through the cervix
Most common causes:
Neisseria gonorrhoeae tends to produce more severe PID
Chlamydia trachomatis
Mycoplasma genitalium
296
Invetsigation markers pelvic inflammatory disease
Pus cells on microscopy. The absence of pus cells is useful for excluding PID.
Raised CRP/ESR
297
Management PID
refer to GUM
A single dose of intramuscular ceftriaxone 1g (to cover gonorrhoea)
Doxycycline 100mg twice daily for 14 days (to cover chlamydia and Mycoplasma genitalium)
Metronidazole 400mg twice daily for 14 days (to cover anaerobes such as Gardnerella vaginalis)
298
Pelvic or lower abdominal pain
Abnormal vaginal discharge
Abnormal bleeding (intermenstrual or postcoital)
Pain during sex (dyspareunia)
Fever
Dysuria
Examination findings may reveal:
Pelvic tenderness
Cervical motion tenderness (cervical excitation)
Inflamed cervix (cervicitis)
Purulent discharge
Patients may have a fever and other signs of sepsis.
PID
299
Presentation lower UTI
dysuria
urinary frequency
urinary urgency
cloudy/offensive smelling urine
lower abdominal pain
fever: typically low-grade in lower UTI
malaise
In elderly patients, acute confusion is a common feature.
300
Investigation lower UTI
1. Urine dip unless
- catheterised
- don't rely on it if woman >65 or man
2. Urine culture if:
- non pregnant woman >65
- non pregnant women visible or non-visible haematuria
- pregnant woman
- man
- symptomatic catheter
301
Management lower UTI
1. Start empirical treatment
2. Review in 48 hours to check response to treatment and to review urine culture results
Non-pregnant
1. trimethorpim or nitrofurantoin for 3 days
2. Nitro if not used 1st or pivmecillinam or fosfomycin single dose
Pregnant
1. Nitrofurantoin (avoid near term) for 7 days
2. amoxicillin or cefalexin for 7 days
Man
1. trimethroprim or nitrofurantoin for 7 days
Symptomatic catheter
1. abx 7 days
+ consider removing or changing catheter if it has bene in for more than 7 days
Haematuria
1. Treat as above
2. Re-test after resolution to consider alt ddx
302
Interpretation of urine dip UTI
urine dip not good at ruling out infection in men, women >65, catheter
Likely:
leuk or nit +
rbc +
Equally likley as other things:
Nit -
Leuk +
= send for culture
Unlikley :
nit -
leuk -
rbc -
= consider other dx
303
management of recurrent UTI
1. Manage acute UTI
2. Refer if ?underlycing cause / ?malignancy
3. Behavioural and personal hygiene measures
Avoid douching
Avoid occlusive underwear
wipe from front to back
Avoid delay of habitual and post-coital urination
Maintain adequate hydration
4. If post-menopausal consider vaginal oestrogen
5. Consider abx prophylaxis
1. Prophylaxis with trimeth or nitro single dose when exposed to a trigger
2. Daily prophylaxis trimeth or nitro
3. Daily prophylaxis amox or cefalexin
Review at 3-6 months
Advise to seek urgent review if sx of UTI - use diff abx to treat
304
at what no of seconds do you interpret rbc, nitrites, leuk urine dip
rbc 60 secs
nitrites 60 secs
leuk 120 secs
305
what could +rbc in urine indicate
urinary tract infection
renal stones
injury to the urinary tract
myoglobinuria (rhabdomyolysis)
nephritic syndrome
malignancy of the urinary tract.
306
what are nitrites in urine, what does it mean?
Nitrites are a breakdown product of gram-negative organisms such as E.Coli
suggests UTI
307
what are leukocyte esterase in urine, what does it indicate?
Leukocyte esterase is an enzyme produced by neutrophils and therefore, when positive, it indicates the presence of white cells in the urine
urinary tract infection
any condition that could result in haematuria
308
what is acute pyelonephritis?
Acute pyelonephritis is an infection of one or both of the kidneys.
It occurs as a result of an ascending urinary tract infection (UTI) which has spread from the bladder up towards the kidneys. It is usually caused by bacteria entering the urinary tract through the urethra.
309
Typical history acute pyleonephritis
- fever
- flank pain usually unilateral
- nausea and vomiting
- haematuria
- foul smelling urine
- malaise
- diarrhoea
- confusion
310
what should you examine for ?acute pyleonephritis
- Tenderness over the loin area
- Signs of shock
Urosepsis is a life-threatening complication of pyelonephritis and can lead to septic shock. Signs include hypotension tachypnoea, skin changes, oliguria
311
how may acute pyelonephirits present at extremes of age?
Young children may have non-specific symptoms such as a fever, irritability and poor feeding
Elderly patients may present with increased confusion or new incontinence.
312
what is urinalysis
urine dip
313
how to make a diagnosis of aucte pyelonephritis?
a definitive diagnosis can be made in patients with loin pain and/or fever if a UTI is confirmed by culturing a urinary pathogen from the urine and other causes of loin pain and/or fever have been excluded.
314
Invetsigations ?acute pyelonephritis
1. Mid-stream urine (MSU) / Catheter specimen urine (CSU)
Consider:
- urinalysis
- blood cultures
- fbc, inflammatory markers etc
Imaging in men, children and recurrent
- USS in children (no radiation, quick)
- CT KUB non-contrast = more sensitive
- MRI in preg women
315
what may an USS for ?acute pylepnephritis show?
May identify obstruction or stones
May identify complications such as perinephric collections and hydronephrosis
316
Management acute pyleonephritis
1. Admit to hospital if:
Severe illness (tachy, hypotension, reduced urine output, tachypnoea, confusion
Severe pain
Not improving after 48 hours in community
Pregnant
Under 3 months or older than 65 years
Underlying diseases: diabetes or abnormality of genitourinary tract
2. IV abx, IV fluids, analgesia, anti-emetics
IV co-amox if younger
IV tazocin if elderly
If community :
7-10 days oral abx : co-amoxiclav, cefalexin, trimethorpim or ciprofloxacin
317
which TB medications can cause hepatitis? how does it present?
RIP
Abdominal pain, nausea, vomiting, unexplained fatigue or jaundice - stop taking and test liver function
318
what are janeway lesions vs oslers nodes? endocarditis
Osler's nodes are on the tip of the finger or toes and painful. O for Owww.
Janeway lesions occur on palm and soles and are non-painful.
319
Management invasive diarrhoea
invasive diarrhoea (causing bloody diarrhoea and fever)
ciprofloxacin
320
management travellers diarrhoea and non-invasive dirrhoea when indicated
Clarithromycin is used for traveller's diarrhoea and non-invasive diarrhoeal illnesses when treatment is necessary.
321
gastroenteritis, stools floating
Giardia causes fat malabsorption, therefore greasy stool can occur
